Changes

Once [[Normal_Mechanisms_of_Haemostatic_Control#Coagulation_physiology|coagulation]] begins a positive feedback loop is set up whereby coagulation inhibitors are consumed, allowing more coagulation. In this way coagulation continues and induces further coagulation.   

Once [[Normal_Mechanisms_of_Haemostatic_Control#Coagulation_physiology|coagulation]] begins a positive feedback loop is set up whereby coagulation inhibitors are consumed, allowing more coagulation. In this way coagulation continues and induces further coagulation.   

Thrombin levels rise; thrombin converts plasminogen into the active form, plasmin which initiates the fibrinolytic cascade. Fibrinolysis produces high levels of fibrin degradation products (FDPs) which are themselves anticoagulants, promoting further coagulation. As thrombi form in the vasculature, tissues become hypoxic leading to multisystemic organ failure in severe cases.   

Thrombin levels rise; thrombin converts plasminogen into the active form, plasmin which initiates the fibrinolytic cascade. Fibrinolysis produces high levels of fibrin degradation products (FDPs) which are themselves anticoagulants, promoting further lysis. As thrombi form in the vasculature, tissues become hypoxic leading to multisystemic organ failure in severe cases.   

As [[Thrombocytes|platelets]] are used up in the thrombi, a [[Platelet Abnormalities#Thrombocytopaenia|thrombocytopaenia]] occurs which leads to paradoxical haemorrhaging and the patient starts to shown symptoms of bleeding.  This is the mechanism by which most viral haemorrahgic diseases induce clinical symptoms.

As [[Thrombocytes|platelets]] are used up in the thrombi, a [[Platelet Abnormalities#Thrombocytopaenia|thrombocytopaenia]] occurs which leads to paradoxical haemorrhaging and the patient starts to shown symptoms of bleeding.  This is the mechanism by which most viral haemorrahgic diseases induce clinical symptoms.